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口腔细菌与远处口腔外部位的漏内皮细胞连接。

Oral bacteria and leaky endothelial junctions in remote extraoral sites.

机构信息

Laboratory of Innate Immunity and Inflammation, Department of Basic and Translational Sciences, University of Pennsylvania, School of Dental Medicine, Philadelphia, PA, USA.

出版信息

FEBS J. 2021 Mar;288(5):1475-1478. doi: 10.1111/febs.15510. Epub 2020 Aug 25.

Abstract

Periodontitis and periodontal pathogens have been associated with systemic complications that influence comorbid conditions, such as cardiovascular disease. Using a zebrafish larvae infection model, Farrugia et al. show that Porphyromonas gingivalis causes vascular damage and increased endothelial permeability by degrading, via its gingipain proteases, platelet endothelial cell adhesion molecule-1, and vascular endothelial cadherin, which are crucial for endothelial junctional integrity. These findings suggest a molecular mechanism whereby this oral pathogen may contribute to endothelial dysfunction and perhaps atherosclerotic cardiovascular disease.

摘要

牙周炎和牙周病原体与全身性并发症有关,这些并发症会影响合并症,如心血管疾病。Farrugia 等人使用斑马鱼幼虫感染模型表明,牙龈卟啉单胞菌通过其牙龈蛋白酶降解血小板内皮细胞黏附分子-1 和血管内皮钙黏蛋白,导致血管损伤和内皮通透性增加,而血小板内皮细胞黏附分子-1 和血管内皮钙黏蛋白对于内皮连接完整性至关重要。这些发现提示了一种分子机制,即这种口腔病原体可能导致内皮功能障碍,甚至可能导致动脉粥样硬化性心血管疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a8a/7904955/2abe61693135/nihms-1644299-f0001.jpg

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